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Matsui, T.

Publications and source records attributed to Matsui, T..

7 recordsLinked to original sources

Astrocytes in the mouse visual cortex reliably respond to visual stimulation

Astrocytes are known to contact with a great number of synapses and may integrate sensory inputs. In the ferret primary visual cortex, astrocytes respond to a visual stimulus with a delay of several seconds with respect to the surrounding neurons. However, in the mouse visual cortex, it remains unclear whether astrocytes respond to visual stimulations. In this study, using dual-color simultaneous in vivo two-photon Ca2+ imaging of neurons and astrocytes in the awake mouse visual cortex, we examined the visual responsiveness of astrocytes and their precise response timing relative to the surrounding neurons. Neurons reliably responded to visual stimulations, whereas astrocytes often showed neuromodulator-mediated global activities, which largely masked small periodic activities. Administration of the selective 1-adrenergic receptor antagonist prazosin substantially reduced such global astrocytic activities without affecting the neuronal visual responses. In the presence of prazosin, astrocytes showed weak but consistent visual responses mostly at their somata. Cross-correlation analysis estimated that the astrocytic visual responses were delayed by approximately 5 s relative to the surrounding neuronal responses. In conclusion, our research demonstrated that astrocytes in the primary visual cortex of awake mice responded to visual stimuli with a delay of several seconds relative to the surrounding neurons, which may indicate the existence of a common mechanism of neuron-astrocyte communication across species.\n\nHighlightsO_LIWe performed dual-color in vivo two-photon Ca2+ imaging of neurons and astrocytes.\nC_LIO_LI1-adrenoblocker prazosin substantially reduced global astrocytic activities.\nC_LIO_LIAstrocytes showed weak but reliable visual responses in the awake mouse visual cortex.\nC_LIO_LIAstrocytic visual responses were delayed by 5 s relative to the neuronal ones.\nC_LI

neuroscience

Molecular typing and macrolide resistance analyses of Treponema pallidumin heterosexuals and men who have sex with men communities in Japan, 2017.

In recent years, syphilis notifications have increased dramatically in Japan. We performed molecular typing and analyzed macrolide resistance of Treponema pallidum samples collected from four clinics and a hospital in Tokyo and Osaka prefectures in 2017.\n\nMacrolide resistant strain type 14d/f was found significantly more in heterosexual syphilis cases compared with those strains identified in men who have sex with men (MSM) syphilis cases. The proportion of 14d/f among heterosexuals was 79% (31/39) compared to 37% (7/19) among MSM [OR, 6.6 (95% CI, 1.7 to 26.7); P=0.002]. 83% (50/60) of the strains were identified as macrolide resistant with an A2058G mutation at the 23S rRNA gene. 90% (35/39) of the heterosexual strains were macrolide resistant, relative to 58% (11/19) of MSM strains; the odds of having the resistant mutation was considerably higher in heterosexuals compared with MSM [OR, 6.4 (95% CI, 1.3 to 33.5); P=0.02]. Heterosexual females and males showed similar distributions, and the results remained the same when restricted to men.\n\nThe strain type distribution and frequency of macrolide resistance differed substantially between heterosexual and MSM syphilis samples, suggesting distinct epidemiologic profiles for the two communities and insight into syphilis transmission dynamics in Japan.

epidemiology

A protocol for an intercomparison of biodiversity and ecosystem services models using harmonized land-use and climate scenarios

Abstract.To support the assessments of the Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES), the IPBES Expert Group on Scenarios and Models is carrying out an intercomparison of biodiversity and ecosystem services models using harmonized scenarios (BES-SIM). The goals of BES-SIM are (1) to project the global impacts of land use and climate change on biodiversity and ecosystem services (i.e. natures contributions to people) over the coming decades, compared to the 20th century, using a set of common metrics at multiple scales, and (2) to identify model uncertainties and research gaps through the comparisons of projected biodiversity and ecosystem services across models. BES-SIM uses three scenarios combining specific Shared Socio-economic Pathways (SSPs) and Representative Concentration Pathways (RCPs) to explore a wide range of land-use change and climate change futures. This paper describes the rationale for scenarios selection, the process of harmonizing input data for land use, based on the second phase of the Land Use Harmonization Project (LUH2), and climate, the biodiversity and ecosystem service models used, the core simulations carried out, the harmonization of the model output metrics, and the treatment of uncertainty. The results of this collaborative modelling project will support the ongoing global assessment of IPBES, strengthen ties between IPBES and the Intergovernmental Panel on Climate Change (IPCC) scenarios and modelling processes, advise the Convention on Biological Diversity (CBD) on its development of a post-2020 strategic plans and conservation goals, and inform the development of a new generation of nature-centred scenarios.

ecology

Noise-resistant developmental reproducibility in vertebrate somite formation

The reproducibility of embryonic development is remarkable, although molecular processes are intrinsically stochastic at the single-cell level. How the multi-cellular system resists the inevitable noise to acquire developmental reproducibility constitutes a fundamental question in developmental biology. Toward this end, we focused on vertebrate somitogenesis as a representative system, because somites are repeatedly reproduced within a single embryo whereas such reproducibility is lost in segmentation clock gene-deficient embryos. However, the effect of noise on developmental reproducibility has not been fully investigated, because of the technical difficulty in manipulating the noise intensity in experiments. In this study, we developed a computational model of ERK-mediated somitogenesis, in which bistable ERK activity is regulated by an FGF gradient, cell-cell communication, and the segmentation clock, subject to the intrinsic noise. The model simulation generated our previous in vivo observation that the ERK activity was distributed in a step-like gradient in the presomitic mesoderm, and its boundary was posteriorly shifted by the clock in a stepwise manner, leading to regular somite formation. Here we showed that this somite regularity was robustly maintained against the noise. Removing the clock from the model predicted that the stepwise shift of the ERK activity occurs at irregular timing with irregular distance owing to the noise, resulting in somite size variation. Through theoretical analysis, we presented a mechanism by which the clock reduces the inherent somite irregularity observed in clock-deficient embryos. Therefore, this study indicates a novel role of the segmentation clock in noise-resistant developmental reproducibility.

developmental biology

Size-reduced embryos reveal a gradient scaling based mechanism for zebrafish somite formation

Little is known about how the sizes of animal tissues are controlled. A prominent example is somite size which varies widely both within an individual and across species. Despite intense study of the segmentation clock governing the timing of somite generation, how it relates to somite size is poorly understood. Here we examine somite scaling and find that somite size at specification scales with the length of the presomitic mesoderm (PSM) despite considerable variation in PSM length across developmental stages and in surgically size-reduced embryos. Measurement of clock period, axis elongation speed, and clock gene expression patterns demonstrate that existing models fail to explain scaling. We posit a \"clock and scaled gradient\" model, in which somite boundaries are set by a dynamically scaling signaling gradient across the PSM. Our model not only explains existing data, but also makes a unique prediction that we experimentally confirm--the formation of periodic \"echoes\" in somite size following perturbation of the size of one somite. Our findings demonstrate that gradient scaling plays a central role both in progression and size control of somitogenesis.\n\nSummary statementBy comparing patterning in zebrafish embryos of different size we show that a dynamically scaling gradient in the presomitic mesoderm regulates somite size control.

developmental biology

Neuronal origin of the temporal dynamics of spontaneous BOLD activity correlation

Resting-state functional connectivity (FC) has become a major fMRI method to study network organization of human brains. There has been recent interest in the temporal fluctuations of FC calculated using short time windows (\"dynamic FC\") because this method could provide information inaccessible with conventional \"static\" FC, which is typically calculated using the entire scan lasting several tens of minutes. Although multiple studies have revealed considerable temporal fluctuations in FC, it is still unclear whether the fluctuations of FC measured in hemodynamics reflect the dynamics of underlying neural activity. We addressed this question using simultaneous imaging of neuronal calcium and hemodynamic signals in mice and found coordinated temporal dynamics of calcium FC and hemodynamic FC measured in the same short time windows. Moreover, we found that variation in transient neuronal coactivation patterns (CAPs) was significantly related to temporal fluctuations of sliding window FC in hemodynamics. Finally, we show that the observed dynamics of FC cannot be fully accounted for by simulated data assuming stationary FC. These results provide evidence for the neuronal origin of dynamic FC and further suggest that information relevant to FC is condensed in temporally sparse events that can be extracted using a small number of time points.

neuroscience

The stress-inducible peroxidase TSA2 enables Chromosome IV duplication to be conditionally beneficial in Saccharomyces cerevisiae

Although chromosomal duplications are often deleterious, in some cases they enhance cells abilities to tolerate specific genetic or environmental challenges. Identifying the genes that cause particular chromosomal duplications to confer these conditionally beneficial effects can improve our understanding of the genetic and molecular mechanisms that enable certain aneuploidies to persist in cell populations and contribute to disease and evolution. Here, we perform a screen for spontaneous mutations that improve the tolerance of haploid Saccharomyces cerevisiae to hydrogen peroxide. Chromosome IV duplication is the most frequent mutation, as well as the only change in chromosomal copy number, seen in the screen. Using a genetic mapping strategy that involves systematically deleting segments of a duplicated chromosome, we show that the Chromosome IV duplications effect is largely due to the generation of a second copy of the stress-inducible cytoplasmic thioredoxin peroxidase TSA2. This finding is consistent with a growing literature indicating that the conditionally beneficial effects of chromosomal duplications tend to reflect the contributions of small numbers of genes that enhance tolerance to specific stresses when their copy number is increased.\n\nArticle summaryChanges in karyotype play an important role in evolution and health. Although these aneuploidization events are usually deleterious, in some instances they show conditionally beneficial effects by enabling cells to tolerate specific mutations or environmental stresses. The mechanisms underlying these protective effects of aneuploidization are not fully understood. To provide insights into this problem, we identify and characterize a conditionally beneficial chromosomal duplication that makes haploid yeast more tolerant to oxidative stress. We determine that the effect of the chromosomal duplication on oxidative stress tolerance is largely explained by duplication of a single stress-inducible gene.

genetics