346 research outputs found

    ザイタク リョウヨウシャ ト カイゴシャ ノ ソウゴ コウイ ブンセキ : アル セキツイ ソンショウシャ ノ キガエ バメン ニ チュウモク シテ

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    Our purpose of this study is to describe a field of home care in detail and to explore the lay knowledge (or body knowledge) and the particularity of the home care. We research the field by interaction analysis. A patient ‘F’ who has paralysis in the lower half of the body and the left upper limbs, permitted us video recording of her everyday life. We especially focus on the scene of (1) “putting on the jacket” and (2) “putting on the gloves (and so on)” with the help of two caregivers (housekeepers) in this paper. As a result of our analysis (1), we find that the caregivers move as if they were F’s hands and that the movements of them are overlapped in about 2 seconds. We also find that there is about 5 seconds interval between taking gloves and putting them on (2). ‘F’ holds out her hands, monitoring the caregivers’ movements one after the other. The F’s body consists in the intercorporeality with the caregivers. As A. Nishizaka suggests ‘the body distributed’, the body counters the distribution though F's body seems to be distributed in home care

    L-BSE prions after propagation in a non-human primate model

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    Classical- (C-) and atypical L-type bovine spongiform encephalopathy (BSE) prions cause different pathological phenotypes in cattle brains, and the disease-associated forms of each prion protein (PrPSc) has a dissimilar biochemical signature. Bovine C-BSE prions are the causative agent of variant Creutzfeldt-Jakob disease. To date, human infection with L-BSE prions has not been reported, but they can be transmitted experimentally from cows to cynomolgus monkeys (Macaca fascicularis), a non-human primate model. When transmitted to monkeys, C- and L-BSE prions induce different pathological phenotypes in the brain. However, when isolated from infected brains, the two prion proteins (PrPSc) have similar biochemical signatures (i.e., electrophoretic mobility, glycoforms, and resistance to proteinase K). Such similarities suggest the possibility that L-BSE prions alter their virulence to that of C-BSE prions during propagation in monkeys. To clarify this possibility, we conducted bioassays using inbred mice. C-BSE prions with or without propagation in monkeys were pathogenic to mice, and exhibited comparable incubation periods in secondary passage in mice. By contrast, L-BSE prions, either with or without propagation in monkeys, did not cause the disease in mice, indicating that the pathogenicity of L-BSE prions does not converge towards a C-BSE prion type in this primate model. These results suggest that, although C- and L-BSE prions propagated in cynomolgus monkeys exhibit similar biochemical PrPSc signatures and consist of the monkey amino acid sequence, the two prions maintain strain-specific conformations of PrPSc in which they encipher and retain unique pathogenic traits

    Identification of the P-TEFb complex-interacting domain of Brd4 as an inhibitor of HIV-1 replication by functional cDNA library screening in MT-4 cells

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    AbstractWe conducted a phenotypic cDNA screening using a T cell line-based assay to identify human genes that render cells resistant to human immunodeficiency virus type 1 (HIV-1). We isolated potential HIV-1 resistance genes, including the carboxy terminal domain (CTD) of bromodomain-containing protein 4 (Brd4). Expression of GFP-Brd4-CTD was tolerated in MT-4 and Jurkat cells in which HIV-1 replication was markedly inhibited. We provide direct experimental data demonstrating that Brd4-CTD serves as a specific inhibitor of HIV-1 replication in T cells. Our method is a powerful tool for the identification of host factors that regulate HIV-1 replication in T cells

    The 1988-1989 explosive eruption of Tokachi-dake, central Hokkaido, Its sequence and mode

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    On December 16, 1988, after 26 years of dormancy since the last eruption in 1962, Tokachi-dake began to erupt from the 62-II crater. The eruption started with phreatic explosions. Then, on December 19, the activity changed into phreatomagmatic explosions of Vulcanian type and continued intermittently until March 5, 1989. Although the composition of the essential ejecta, mafic andesite, is similar to those of 1926 and 1962 eruptions, the mode of the present eruption is considerably diffrent The present eruption consists of a series of 23 discrete cannon-like explosions, being frequently accompanied with small-scale pyrcclastic surges and flows. The total volume of ejecta amounts to approximately 6×105 m3, of which about 20% is essential ejecta. A complete sequence of events was compiled and distribution maps of the ash-fall, ballistic blocks, and pyroclastic surges and flows were drawn for each of the larger eruptions. The pyrrolastic surges and flows of the present eruption were small scale, low temperature pyroclastic flows, rich in accessory clasts and unaccompanied by sector collapse. Therefore, the sudden melting of snow causing disastrous mudflows, as in the case of the 1926 eruption, fortunately did not occur

    Chtop (Chromatin target of Prmt1) auto-regulates its expression level via intron retention and nonsense-mediated decay of its own mRNA

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    Chtop (chromatin target of Prmt1) regulates various aspects of gene expression including transcription and mRNA export. Despite these important functions, the regulatory mechanism underlying Chtop expression remains undetermined. Using Chtop-expressing human cell lines, we demonstrate that Chtop expression is controlled via an autoregulatory negative feedback loop whereby Chtop binds its own mRNA to retain intron 2 during splicing; a premature termination codon present at the 5′ end of intron 2 leads to nonsense-mediated decay of the mRNA. We also show that Chtop interacts with exon 2 of Chtop mRNA via its arginine-glycine-rich (RG) domain, and with intron 2 via its N-terminal (N1) domain; both are required for retention of intron 2. In addition, we show that hnRNP H accelerates intron 2 splicing of Chtop mRNA in a manner dependent on Chtop expression level, suggesting that Chtop and hnRNP H regulate intron 2 retention of Chtop mRNA antagonistically. Thus, the present study provides a novel molecular mechanism by which mRNA and protein levels are constitutively regulated by intron retention

    宙返り技の動感形態化に関する超越論的静態分析的一考察

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    Attaining refinement and stabilization of motor skills is indispensable to advanced performance in athletics training. When coaches lead gymnasts to a higher performance level, they need to have a flair for fine coordinated movement; in other words, there is a need for kinesthetic information on high-performance movement. However, no previous studies have clarified the characteristics of kinesthetic genesis and structure during the learning process in advanced classes. This paper focuses on the genesis of kinesthetic sensations centering on the somersault techniques of advanced gymnasts. Therefore, phenomenological transcendental static analysis was employed to clarify the kinesthetic sensations related to “swing backward to double sault forward tucked” on uneven bars. This analysis clarified the typical structures of the kinesthetic consciousness of gymnasts who have attained the refined and stabile movement form of “swinging backward to double sault forward tucked” on uneven bars, and the present results may serve as a guide for coaching to attain fine coordination and stabilization

    Poly(A)-specific ribonuclease regulates the processing of small-subunit rRNAs in human cells

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    Ribosome biogenesis occurs successively in the nucleolus, nucleoplasm, and cytoplasm. Maturation of the ribosomal small subunit is completed in the cytoplasm by incorporation of a particular class of ribosomal proteins and final cleavage of 18S-E pre-rRNA (18S-E). Here, we show that poly(A)-specific ribonuclease (PARN) participates in steps leading to 18S-E maturation in human cells. We found PARN as a novel component of the pre-40S particle pulled down with the pre-ribosome factor LTV1 or Bystin. Reverse pull-down analysis revealed that PARN is a constitutive component of the Bystin-associated pre-40S particle. Knockdown of PARN or exogenous expression of an enzyme-dead PARN mutant (D28A) accumulated 18S-E in both the cytoplasm and nucleus. Moreover, expression of D28A accumulated 18S-E in Bystin-associated pre-40S particles, suggesting that the enzymatic activity of PARN is necessary for the release of 18S-E from Bystin-associated pre-40S particles. Finally, RNase H–based fragmentation analysis and 3΄-sequence analysis of 18S-E species present in cells expressing wild-type PARN or D28A suggested that PARN degrades the extended regions encompassing nucleotides 5–44 at the 3΄ end of mature 18S rRNA. Our results reveal a novel role for PARN in ribosome biogenesis in human cells

    Developmental Trajectory of Infant Brain Signal Variability: A Longitudinal Pilot Study

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    The infant brain shows rapid neural network development that considerably influences cognitive and behavioral abilities in later life. Reportedly, this neural development process can be indexed by estimating neural signal complexity. However, the precise developmental trajectory of brain signal complexity during infancy remains elusive. This study was conducted to ascertain the trajectory of magnetoencephalography (MEG) signal complexity from 2 months to 3 years of age in five infants using multiscale entropy (MSE), which captures signal complexity at multiple temporal scales. Analyses revealed scale-dependent developmental trajectories. Specifically, signal complexity predominantly increased from 5 to 15 months of age at higher temporal scales, whereas the complexity at lower temporal scales was constant across age, except in one infant who showed decreased complexity. Despite a small sample size limiting this study’s power, this is the first report of a longitudinal investigation of changes in brain signal complexity during early infancy and is unique in its application of MSE analysis of longitudinal MEG data during infancy. The results of this pilot study may serve to further our understanding of the longitudinal changes in the neural dynamics of the developing infant brain

    Characterisation of Ppy-lineage cells clarifies the functional heterogeneity of pancreatic beta cells in mice

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    Aims/hypothesis Pancreatic polypeptide (PP) cells, which secrete PP (encoded by the Ppy gene), are a minor population of pancreatic endocrine cells. Although it has been reported that the loss of beta cell identity might be associated with beta-to-PP cell-fate conversion, at present, little is known regarding the characteristics of Ppy-lineage cells. Methods We used Ppy-Cre driver mice and a PP-specific monoclonal antibody to investigate the association between Ppy-lineage cells and beta cells. The molecular profiles of endocrine cells were investigated by single-cell transcriptome analysis and the glucose responsiveness of beta cells was assessed by Ca2+ imaging. Diabetic conditions were experimentally induced in mice by either streptozotocin or diphtheria toxin. Results Ppy-lineage cells were found to contribute to the four major types of endocrine cells, including beta cells. Ppy-lineage beta cells are a minor subpopulation, accounting for 12–15% of total beta cells, and are mostly (81.2%) localised at the islet periphery. Unbiased single-cell analysis with a Ppy-lineage tracer demonstrated that beta cells are composed of seven clusters, which are categorised into two groups (i.e. Ppy-lineage and non-Ppy-lineage beta cells). These subpopulations of beta cells demonstrated distinct characteristics regarding their functionality and gene expression profiles. Ppy-lineage beta cells had a reduced glucose-stimulated Ca2+ signalling response and were increased in number in experimental diabetes models. Conclusions/interpretation Our results indicate that an unexpected degree of beta cell heterogeneity is defined by Ppy gene activation, providing valuable insight into the homeostatic regulation of pancreatic islets and future therapeutic strategies against diabetes
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