737 research outputs found

    Syntheses of Technetium β-Diketone and 8-Quinolinol Complexes

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    開始ページ、終了ページ: 冊子体のページ付

    Comparison of the Effects of Two Types of Stretching Warm Ups for Rehabilitation

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    This pilot study compares the effects of static therapeutic trunk stretching using an unstable flex chair, a stretching bench and a stretching stick on physical fitness with those of a general Japanese style of static stretching. The participants underwent physical fitness tests. Before and after warming up using a general Japanese style of stretching and trunk treatment stretching. Twenty-three healthy college students (age, 20.7 ± 1.2 years; height, 165.3 ± 7.6 cm; weight, 59.0 ± 9.7 kg; BMI 21.4 ± 2.3) were enrolled in this study. The physical fitness test assesses grip strength, sit-ups, eyes-closed single-leg stance, sit-and-reach flexibility, six-minute walk, and ten-meter obstacle course. The participants performed vertical jump, forward standing flexion measured using the analog flexion meter, thoracolumbar extension, horizontal flexure, deep forward bow. These results suggest that trunk stretching improves flexibility, walking ability, endurance and explosive power more effectively than the general Japanese style of stretching. Three static trunk stretches can improve flexibility, walking ability, endurance and explosive power. Trunk treatment stretching before physical activity might reduce the incidence of injury and improve the physical performance of individuals who participate in exercise, athletes and injured persons undergoing rehabilitation.ArticleBAOJ Medical and nursing.1(1):003(2015)journal articl

    Degradation of human kininogens with the release of kinin peptides by extracellular proteinases of Candida spp.

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    The secretion of proteolytic enzymes by pathogenic microorganisms is one of the most successful strategies used by pathogens to colonize and infect the host organism. The extracellular microbial proteinases can seriously deregulate the homeostatic proteolytic cascades of the host, including the kinin-forming system, repeatedly reported to he activated during bacterial infection. The current study assigns a kinin-releasing activity to secreted proteinases of Candida spp. yeasts, the major fungal pathogens of humans. Of several Candida species studied, C. parapsilosis and C. albicans in their invasive filamentous forms are shown to produce proteinases which most effectively degrade proteinaceous kinin precursors, the kininogens. These enzymes, classified as aspartyl proteinases, have the highest kininogen-degrading activity at low pH (approx. 3.5), but the associated production of bradykinin-related peptides from a small fraction of kininogen molecules is optimal at neutral pH (6.5). The peptides effectively interact with cellular B2-type kinin receptors. Moreover, kinin-related peptides capable of interacting with inflammation-induced B1-type receptors are also formed, but with a reversed pH dependence. The presented variability of the potential extracellular kinin production by secreted aspartyl proteinases of Candida spp. is consistent with the known adaptability of these opportunistic pathogens to different niches in the host organism

    Moderate exercise improves cognitive performance and decreases cortical activation in the go/no-go task

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    Background: A lot of studies have reported that physical activity has a beneficial influence not only on physical and mental disorders but also on cognitive and brain function. Performance of a go/no-go task improves after exercise. However, few studies have compared neural activity in a go/no-go task performed before and after exercise to identify brain regions that may respond to exercise and underlie this result. Therefore, the purpose of this study was to examine the brain blood flow and compare the cortical activation pattern during a go/no-go task performed before and after exercise.Method: Fifteen healthy subjects performed a go/no-go task before and after exercise. Functional near-infrared spectroscopy (fNIRS) was used to measure oxygenated hemoglobin concentration at 44 locations over both hemispheres. The exercise was of moderate intensity, defined as 50% of peak oxygen uptake.Result: The reaction time on the go/no-go task was significantly faster after exercise than before. The oxygenated hemoglobin concentration quantified across the whole brain was lower after exercise, and this was the case for go trials and no-go trials. In go trials, the oxygenated hemoglobin concentration in dorsolateral prefrontal cortex and supplementary motor area were significantly lower after exercise.Conclusion: These results suggest that the dorsolateral prefrontal cortex and supplementary motor area had lower activity in go trials in the go/no-go task performed after exercise than in go trials in the go/no-go task performed before exercise.ArticleBAOJ Medical and nursing.1(1):002(2015)journal articl

    Three-dimensional femtosecond laser nanolithography of crystals

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    Nanostructuring hard optical crystals has so far been exclusively feasible at their surface, as stress induced crack formation and propagation has rendered high precision volume processes ineffective. We show that the inner chemical etching reactivity of a crystal can be enhanced at the nanoscale by more than five orders of magnitude by means of direct laser writing. The process allows to produce cm-scale arbitrary three-dimensional nanostructures with 100 nm feature sizes inside large crystals in absence of brittle fracture. To showcase the unique potential of the technique, we fabricate photonic structures such as sub-wavelength diffraction gratings and nanostructured optical waveguides capable of sustaining sub-wavelength propagating modes inside yttrium aluminum garnet crystals. This technique could enable the transfer of concepts from nanophotonics to the fields of solid state lasers and crystal optics.Comment: Submitted Manuscript and Supplementary Informatio

    The Effect of Epstein-Barr Virus Latent Membrane Protein 2 Expression on the Kinetics of Early B Cell Infection

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    Infection of human B cells with wild-type Epstein-Barr virus (EBV) in vitro leads to activation and proliferation that result in efficient production of lymphoblastoid cell lines (LCLs). Latent Membrane Protein 2 (LMP2) is expressed early after infection and previous research has suggested a possible role in this process. Therefore, we generated recombinant EBV with knockouts of either or both protein isoforms, LMP2A and LMP2B (Δ2A, Δ2B, Δ2A/Δ2B) to study the effect of LMP2 in early B cell infection. Infection of B cells with Δ2A and Δ2A/Δ2B viruses led to a marked decrease in activation and proliferation relative to wild-type (wt) viruses, and resulted in higher percentages of apoptotic B cells. Δ2B virus infection showed activation levels comparable to wt, but fewer numbers of proliferating B cells. Early B cell infection with wt, Δ2A and Δ2B viruses did not result in changes in latent gene expression, with the exception of elevated LMP2B transcript in Δ2A virus infection. Infection with Δ2A and Δ2B viruses did not affect viral latency, determined by changes in LMP1/Zebra expression following BCR stimulation. However, BCR stimulation of Δ2A/Δ2B cells resulted in decreased LMP1 expression, which suggests loss of stability in viral latency. Long-term outgrowth assays revealed that LMP2A, but not LMP2B, is critical for efficient long-term growth of B cells in vitro. The lowest levels of activation, proliferation, and LCL formation were observed when both isoforms were deleted. These results suggest that LMP2A appears to be critical for efficient activation, proliferation and survival of EBV-infected B cells at early times after infection, which impacts the efficient long-term growth of B cells in culture. In contrast, LMP2B did not appear to play a significant role in these processes, and long-term growth of infected B cells was not affected by the absence of this protein. © 2013 Wasil et al

    Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

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    Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors
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